Pediatr Transplantation 2015: 19: 261–266
© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Pediatric Transplantation DOI: 10.1111/petr.12429
Technique advance to avoid hepatic venous outﬂow obstruction in pediatric living-donor liver transplantation Tannuri U, Tannuri ACA, Santos MM, Miyatani HT. (2015) Technique advance to avoid hepatic venous outﬂow obstruction in pediatric living-donor liver transplantation. Pediatr Transplant, 19: 261–266. DOI: 10.1111/petr.12429. Abstract: HVOO represents a serious critical complication of pediatric living-donor liver transplantation because open surgical repair is virtually impossible. Currently, despite several technical innovations and the introduction of triangulated anastomosis for hepatic vein reconstruction, the reported incidence of HVOO is still considerable. The aim of this study was to propose a new technique for hepatic venous reconstruction that avoids the original oriﬁce of the recipient hepatic veins. Instead, anastomosis is performed in a newly created wide longitudinal oriﬁce in the anterior wall of the recipient inferior vena cava. A total of 210 living related-donor liver transplantations were performed using two methods for reconstruction of the hepatic vein. Group 1 included 69 patients subjected to direct anastomosis of the oriﬁce of the graft hepatic vein and a wide oriﬁce created in the recipient inferior vena cava by the conﬂuence of the oriﬁces of the right, left, and middle hepatic veins. Group 2 included 141 patients in whom the original oriﬁces of the recipient hepatic veins were closed, the inferior vena cava was widely opened, and a long longitudinal anastomosis was performed using two lines of continuous sutures. Diagnosis of HVOO was suspected based on clinical ﬁndings and ultrasound studies and then conﬁrmed by liver biopsy and interventional radiology examinations. Among the 69 recipients in group 1, 16 patients died due to graft problems during the postoperative period and eight of the survivors (15.1%) presented with HVOO. In group 2 (141 patients), 21 patients died, and there were no cases of HVOO. A comparison of the incidence of HVOO between groups revealed a signiﬁcant diﬀerence (p = 0.01). Hepatic venous reconstruction during pediatric living-donor liver transplantation should be performed using a wide longitudinal incision in the anterior wall of the recipient inferior vena cava because this technique eliminated anastomosis complications.
Most centers that perform pediatric liver transplantation have been challenged by the devastating complication of HVOO, with an incidence of 0.8–10.5% according to the recent publications (1–4). This problem is critical because open surgical repair is virtually impossible, unlike portal
Abbreviations: HTK, histidine-tryptophan-ketoglutaratex; HVOO, hepatic venous outﬂow obstruction; MMF, mofetil mycophenolate; PELD, pediatric end-stage liver disease.
Uenis Tannuri, Ana Cristina A. Tannuri, Maria M. Santos and Helena T. Miyatani Liver Transplantation Unit, Children’s Institute, University of Sao Paulo, Sao Paulo, Brazil
Key words: living-donor liver transplantation – hepatic venous obstruction – pediatric liver transplantation – donor hepatectomy – complications of liver transplantation Uenis Tannuri, Faculdade de Medicina da Universidade de S~ao Paulo, Avenida Dr. Arnaldo 455, 4° andar, sala 4106, S~ao Paulo – SP, CEP: 01246-903, Brazil Tel.: 0055 11 30812943 Fax: 0055 11 32556285 E-mail: [email protected]
[The copyright line for this article was changed on 17th March 2015 after original online publication] Accepted for publication 17 December 2014
or arterial reconstructions that permit corrective operations. Initially, HVOO was not a problem in liver transplantation cases because adult and pediatric whole-liver transplantations were regularly performed using suprahepatic cavocaval terminoterminal anastomosis. In cases of wholeliver and cadaveric reduced-size or living-donor liver transplants, the incidence of HVOO was as high as 27.7% following introduction of the piggyback technique for hepatic vein reconstruc tion (5). In addition to the technical problems 261
Tannuri et al.
associated with hepatic vein reconstruction and/ or subsequent ﬁbrosis of the anastomosis line, another cause of HVOO is twisting of the anastomosis due to graft growth and its location within the recipient liver fossa (6). Despite several technical innovations and the introduction of triangulated anastomosis for hepatic vein reconstruction in cases of living-donor pediatric transplantation, the reported incidence of HVOO is still considerable. Our program for living related-donor liver transplantation began in 1998, and the outﬂow reconstruction technique was based on a direct end-to-end anastomosis of the recipient and donor hepatic veins. Although this technique appeared to be anatomically and technically sound, it was ultimately inadequate because a high incidence of HVOO was observed, despite the wide outﬂow oriﬁce created for anastomosis. In addition, treating this complication proved to be complex and exclusively dependent on interventional radiology. Therefore, we proposed to prospectively study a new technique for hepatic venous reconstruction that avoids using the original oriﬁce of the recipient hepatic veins. Instead, the anastomosis was performed in a newly created wide longitudinal oriﬁce in the anterior wall of the recipient inferior vena cava. Patients and methods From July 1998 to June 2014, 585 consecutive pediatric liver transplantations were performed at the Liver Transplantation Unit of the Children Institute (University of Sao Paulo School of Medicine). Of these cases, 210 involved living related-donor liver transplantation. The donors included 101 fathers, 83 mothers, eight uncles, six cousins, four brothers, one grandmother, one grandfather, and six nonrelatives, with a median age of 29 yr (range, 19–50 yr). The indications for transplantation are listed in Table 1. There were 83 male and 127 female recipients whose ages ranged from six months to 16 yr. The screening for donor selection included a complete clinical evaluation, blood chemistry analysis, blood count
Table 1. Indications for living-donor liver transplantation Disease
Number of patients
Biliary atresia Fulminant hepatic failure Cryptogenic cirrhosis Alpha 1 antitrypsin deficiency Primary sclerosing colangitis Hepatoblastoma Congenital hepatic fibrosis Alagille’s syndrome Tirosinemia Autoimmune hepatitis Others
134 24 11 8 7 6 4 4 3 2 7
and testing for viral hepatitis, and other infectious diseases. The selected donors underwent a preoperative imaging examination that consisted of a complete ultrasound examination with Doppler study and angiotomography to obtain a thorough hepatic vascular imaging study. During the three-ﬁrst years at the center, arteriography was used to evaluate the arterial and venous supply to the liver; however, this technique was abandoned after the introduction of angiotomography. The patency of the hepatic veins, inferior vena cava, and portal vein of the recipients was also conﬁrmed using Doppler ultrasound. All of the donors were operated on by the same team of pediatric surgeons, and the recipient procedures were all performed by the same surgeon (a senior surgeon – the ﬁrst author). The donor and recipient procedures were simultaneously performed in two juxtaposed operating rooms that had been speciﬁcally adapted for these procedures. The donor operation began ﬁrst, except in cases of unresectable malignant hepatic tumors in the recipient. After anesthesia induction, central and peripheral venous lines, invasive pressure monitoring by catheterization of the left radial artery and installation of an epidural catheter for perioperative analgesia for 24–48 h were completed. After the donor liver was inspected and judged to be satisfactory, the recipient operation commenced to minimize the cold ischemia time. A bilateral subcostal incision was preferred because it enabled proper exposure of the operative ﬁeld and an acceptable cosmetic appearance. A similar incision was performed on the recipient patient. The left lobe was fully mobilized by sectioning the falciform and left triangular ligaments. Prior to any dissection of the hepatic hilum, all vascular anomalies were carefully investigated. In the ﬁrst 20 transplantations, the entire hilum was dissected to identify the arterial and portal venous supplies. Subsequently, the dissection was conﬁned to the left branch of the portal vein and the left hepatic artery, and minimal dissection was performed around the left hepatic duct to avoid damaging its blood supply. In the single case of right lobe donation, the right branch of the portal vein, right hepatic artery, and retro hepatic inferior vena cava were dissected and liberated from the liver. The hepatectomies were performed without clamping the portal triad, and the vessels were divided after completing parenchyma dissection. All donors underwent a cholecystectomy and intra-operative cholangiography to identify the anatomy of the biliary tree. Hepatic parenchyma sectioning was performed under the guidance of an ultrasonic surgical aspirator (CUSAâ – Integra Life Sciences, Plainsboro, NJ, USA), LigaSureâ (Valleylab, Louisville, KY, USA) and electrocautery using the liver-hanging maneuver. An additional graft of the donor inferior mesenteric vein was harvested to replace a hypoplastic recipient portal vein in 10 donors. All donors had a Jackson-Prattâ or Blakeâ drain inserted in the abdominal cavity around the cut surface of the liver that was maintained for a median of four days. The liver grafts included the left lateral segment and the left hepatic vein in 170 patients. The extended left lateral segment, which always included the left and middle hepatic veins, was grafted in 39 patients. The right hepatic lobe was used in one patient. After harvesting, the liver segment was weighed, and the hepatic veins were carefully inspected. Graft ﬂushing was performed with University of Wisconsin solution until it was replaced by HTK solution in June 2009. When necessary, venoplasty of the hepatic vein oriﬁces was performed. When the left and middle hepatic veins
HVOO in liver transplantation were included in the graft, venoplasty was performed using interrupted 6-0 prolene sutures with knots on the extraluminal side to create a large single oriﬁce. The grafted hepatic vein was cut short, and its oriﬁce was always enlarged with a longitudinal incision into the posterior surface of the vein to allow duplication of its diameter (7). In the recipients, total hepatectomies were performed using classical techniques with preservation of the inferior vena cava and no application of venovenous bypass. Two clamps were used to clamp the inferior vena cava at the supraheptic and infrahepatic areas. Two methods were applied to reconstruct the hepatic vein. In the ﬁrst 69 patients (group 1), we used direct anastomosis of the grafted hepatic vein oriﬁce and the wide oriﬁce created in the recipient inferior vena cava by the conﬂuence of the oriﬁces of the right, left, and middle hepatic veins. In many patients, the wide oriﬁce was triangulated with an additional incision at the anterior wall of the inferior vena cava. The anastomoses were performed using continuous 5-0 prolene sutures in all cases. In group 2 (141 patients), the original oriﬁces of the hepatic veins were closed using continuous 5-0 prolene sutures. The anterior wall of the inferior vena cava was widely opened (Fig. 1a), and a long longitudinal anastomosis was easily performed using two lines of continuous 5-0 prolene sutures. The graft was positioned so that the entire raw surface faced the right side (Fig. 1b). After hepatic vein reconstruction, the portal vein was anastomosed to the trunk of the recipient’s portal vein in an end-to-end fashion using continuous 6-0 sutures.
Fig. 1. (a) Incision in the anterior wall of the inferior vena cava. Note the wide oriﬁce created. (b) Final aspect of the anastomosis. Note that the graft becomes ﬁrmly attached to the anterior wall of the inferior vena cava, without possibility of twisting.
The graft was reperfused after completion of the portal vein anastomosis, and microsurgical reconstruction of the artery was then performed. Until 2011, the hepatic artery of the graft liver was anastomosed to one of the stumps of the main branches or trunk of the proper hepatic artery of the recipient in an end-to-end fashion using 8-0 or 9-0 prolene sutures and a surgical microscope (magniﬁcation 89). After 2011, surgical loupes (magniﬁcation 39) were used. Lastly, bile duct reconstruction was performed using a Roux-en-Y limb of the jejunum. When necessary, the falciform ligament was additionally sutured anteriorly to the diaphragm immediately before closing the abdominal wall to promote stabilization of the graft position and prevent subsequent graft rotation. During the postoperative period, anticoagulation therapy consisted of intravenous dextran-40 (0.5 mL/kg/h) for the ﬁrst 60 patients, followed by oral persantin when possible. Over the past few years, dextran-40 has not been administered because it is not available in our country. As previously reported, heparin (150 U/kg/day) was added when indicated by the INR prothrombin time (below 3.0). Immunosuppression was achieved using a calcineurin inhibitor, with cyclosporine administered from 1989 to 2000 and tacrolimus thereafter. Every child received methylprednisolone (20 mg/kg) at the time of graft reperfusion. Corticosteroids were gradually tapered during the postoperative period to a maintenance dosage of 0.5–1.0 mg/kg of body weight/day. A third drug, MMF, was added only in cases involving repeated episodes of rejection or refractory rejection. MMF and sirolimus were also used as single-drug immunosuppressants in patients who presented with deterioration in renal function. OKT3 or thymoglobulin was administered to children presenting with steroid-resistant rejection. Routine liver function tests were performed to monitor graft function, and a liver biopsy was performed when indicated. The patients were followed for periods ranging from three months to 16 yr. A diagnosis of HVOO was suspected based on clinical ﬁndings and ultrasound imaging. Clinical signs included ﬂuid retention manifesting with ascites or pleural eﬀusion, persistent hyponatremia, lower extremity edema, and hepatomegaly. Ultrasound images of hepatic vein stenosis were conﬁrmed using pre- and post-vein anastomosis ﬂow rate studies. Upon suspicion of HVOO, a liver biopsy was taken. When histological changes suggested outﬂow obstruction, a venogram of the inferior vena cava was obtained to assess the hepatic veins. Venograms were performed under general anesthesia. Initially, the right internal jugular vein was entered with a 5 Fr coaxial micropuncture introducer set (Cook, Bloomington, IN, USA). Images of the inferior vena cava were obtained using a 5 Fr pigtail catheter, and selective catheterization of the hepatic veins was performed using a 5 Fr catheter and a hydrophilic Terumo guide wire (Terumo Corporation, Tokyo, Japan). After identifying the site of stenosis and evaluating the gradient pressure, three dilatations were performed using a 10 9 20 or 12 9 20 mm balloon (Med-tech/Boston Scientiﬁc, Watertown, MA, USA) according to the diameter of the hepatic vein. In cases of relapsing stenosis that required more than two sessions of dilatation, a balloon expandable metal stent was placed at the site of the stenosis. Comparisons between the groups were performed using the chi-square method. The results were considered signiﬁcant at p < 0.05.
Tannuri et al. Results
No donor mortality occurred in this series, and all 210 living donors remain alive to date. However, adverse events were reported for 25 patients (11.9%), including nine with abdominal pain and severe gastrointestinal symptoms due to transitory gastric dysmotility. A total of ﬁve donors with adverse symptoms required re-operation. One donor returned to the operative room in the immediate postoperative period due to bleeding at the left hepatic vein suture site, with hemodynamic repercussion and the need for transfusion of red cells. Two donors had adhesions causing gastric outlet obstruction and two other donors underwent re-operation because of a bile leak into the peritoneal cavity. A total of nine donors had minor bile leaks that were treated conservatively. Three donors developed extraperitoneal infections (one incision abscess, one peripheral phlebitis, and one pneumonia). The long-term follow-up of patients ranged from four months to 94 months (median, 66 months) and revealed that all of the patients are living well without symptoms. Among the 69 recipients of group 1, a total of 16 patients were excluded due to graft problems during the early postoperative period (ﬁve deaths due to hepatic artery thrombosis, two deaths due to portal vein thrombosis, one death due to early acute arterial and portal vein thrombosis, and eight successful retransplantations because of hepatic artery thrombosis). The remaining 53 patients experienced successful postoperative recovery. Among these patients, nine presented with clinical evidence of HVOO that was conﬁrmed by liver biopsy. In eight (15.1%) of these children, the angiographic imaging studies revealed the presence of a high-grade stricture at the site of the hepatic vein anastomosis with stagnation of the contrast injected into the hepatic veins. In one patient, no evidence of stenosis or pressure gradients was found in the angiography. All eight patients underwent two or three sessions of balloon dilatations of the anastomoses. These procedures proved successful in only four children (4/8, 50.0%). In the remaining four patients, a metal stent (Palmaz P-188) was applied at the site of the stenosis and dilated up to 12 mm in luminal diameter in the anastomosis because of recurring ascites, lower extremity edema and hyponatremia. In all cases, these signals resolved within 3–5 days of stent placement. After two wk, ultrasound examination revealed a widely patent stent, normal ﬂow, and waveforms in the hepatic veins and no evidence of ascites. Two of these patients remained well and 264
showed no evidence of HVOO; however, one patient presented with the serious complication of stent migration to the right pulmonary artery. Another patient presented with a recurrence of ascites, graft enlargement, and lower extremity edema, and a new venography indicated obstruction of the inferior vena cava close to the right atrium, suggesting graft rotation. This complication was treated using a second metal stent across this stricture. Five months after stent placement, this patient died from a monomorphic form of lymphoproliferative disorder. In the children with HVOO, histopathological ﬁndings included moderate to severe congestive changes in zone 3 with dilatation of both the central vein and sinusoids. In addition to these congestive changes, other ﬁndings included moderate ﬁbrosis in zone 3 or the centrilobular necrosis of hepatocytes. These changes were completely reversed by the placement of the metal stent. In group 2, 21 patients (14.9%) died from problems related to the transplantation. Three patients in this group presented with clinical signs that suggested HVOO; however, this condition was not conﬁrmed by either ultrasound examination or radiological intervention. In each of these three cases, the catheter was easily introduced into the hepatic veins via the right atrium during radiological intervention. The images demonstrated a wide hepatic vein anastomosis and no blood stasis in the liver parenchyma (Fig. 2). Therefore, it was concluded that none of the patients in this group presented any kind of HVOO. A comparison of the incidence of HVOO between the groups revealed a signiﬁcant diﬀerence (p = 0.01). Discussion
Although the available literature describes complication rates in living graft donors for transplants ranging from 3.2% to 67.0% of patients and a few reports of donor deaths with an estimated rate of 0.1–0.3% (8, 9), the present series revealed a low incidence of complications in the living liver donors. Fortunately, the indices associated with pediatric liver transplantation are smaller, and the morbidities are less severe due to the high number of grafts involving the lateral segment or left lobe. Similar to previous reports, adverse events in the current series occurred in 11.9% of patients. All patients developed anticipated complications in cases involving liver resections, and the majority showed complete recovery from these symptoms within 30 days. However, ﬁve patients required re-operations. In
HVOO in liver transplantation
Fig. 2. Venogram of hepatic vein-inferior vena cava anastomosis. Note the wide anastomosis and lack of blood stasis in the liver parenchyma.
addition, the low incidence of complications could be attributed to a meticulous preoperative evaluation that excluded all donor candidates who presented with any clinical or laboratory alterations. The current series shows a relatively high incidence of mortality (14.9% in the second group). The main causes were the bad clinical conditions of the recipients, presenting with high PELD scores and hypoplastic portal vein, mainly in small children with biliary atresia. This last problem has been corrected using a graft of the donor inferior mesenteric as a substitute for the hypoplastic portal vein (unpublished data). With respect to HVOO, the incidence following pediatric liver transplantation has been increasing in clinical practice because classical whole-liver transplantation has been replaced with reduced-size cadaveric or living-donor liver transplantation. In the current series (unpublished observation) and in other reported experiences, whole-liver transplantations in children represent only 10–25% of all cases (10, 11). Consequently, anastomotic stricture of the hepatic veins has been described as a serious complication in pediatric patients because of the reduced caliber of the hepatic veins compared with those of adults. Children typically receive small hepatic segments from a living donor or a reduced or split cadaveric graft, which carry a higher risk of graft rotations and positional changes. In fact, HVOO is more reported in children than in adult patients. As we have shown in the current series, the diagnosis of HVOO is based on clinical signs, ultrasound examination, and pathological
features and is conﬁrmed by venogram of the inferior vena cava. In the majority of cases, pathological features indicative of inferior vena cava imaging study include moderate to severe congestive changes in zone 3, with dilatation of the central vein and of the sinusoids. Nevertheless, it was observed that in malnourished liver transplanted pediatric patients, HVOO may be pathologically manifested by isolated centrilobular necrosis, sometimes erroneously interpreted as severe acute cellular rejection (12). Unlike portal vein obstruction, a signiﬁcant problem associated with HVOO is that surgical intervention to completely correct the obstruction is not possible. The only treatment for HVOO is dilatation of the stenosed anastomosis through radiology intervention. Alternatively, a metal stent can be inserted in some cases. Despite the eﬃcacy of these techniques, complete regression of symptoms, and reversal of pathological ﬁndings, some patients may develop severe graft dysfunction that leads to complete graft loss. In fact, Sakamoto et al., reported the case of a child who lost her liver graft despite adequate correction of an HVOO using interventional radiology. After venous outﬂow decompression, centrilobular injuries were replaced by massive obliterative lesions of central venules that caused an irreversible venous occlusive disease treated by retransplantation (6). The best surgical technique to reconstruct hepatic venous anastomosis remains controversial. Thus, we report our current series results that indicate an elimination of HVOO. When performing hepatic vein reconstruction, the creation of a wide longitudinal incision at the anterior wall of the inferior vena cava is important. In addition, the size of the anastomotic oriﬁce must be enlarged by performing a longitudinal incision into the posterior surface of the graft vein, and the orientation of the vessels and the position of the graft must be arranged to allow the entire raw surface of the graft to face the right side. These features strongly aﬀect the ability to maintain patency of the reconstructed hepatic veins. According to the classical recommendations for hepatic outﬂow reconstruction in liver transplantations of children and babies, we used continuous 5-0 monoﬁlament non-absorbable sutures in all cases. In the ﬁrst group of patients, we performed a direct end-to-end anastomosis between the enlarged oriﬁce of the donor hepatic veins and the original common oriﬁces of the recipient hepatic veins. However, we observed that 15.1% of the patients developed HVOO, an incidence similar to previously reported cases of reduced-size liver transplantation (4, 13, 14). 265
Tannuri et al.
Therefore, we sought to create a novel technique that would eliminate this type of complication. In the ﬁrst group of patients, the most commonly reported techniques for hepatic vein reconstruction were used. In addition to stenosis at the anastomosis line, another serious complication was graft rotation at the level of anastomosis that severely compromised blood outﬂow from the liver. When performing hepatic vein reconstructions, we could verify that the risk of this complication was increased when the recipient hepatic vein oriﬁces were used, particularly in patients presenting with a previously large volume of liver parenchyma and a large hepatic fossa, because the small graft was then able to freely rotate to the right side. Thus, the anastomosis must be designed to allow the graft to rest comfortably within the hepatic fossa after abdominal closure without twisting the graft hepatic vein at the line of the anastomosis. The technique performed on the second group of patients aimed to eliminate this complication, because the original oriﬁces of the recipient hepatic vein were not utilized, and the graft was anastomosed closely to the entire anterior wall of the inferior vena cava. After completion of anastomosis, the graft becomes ﬁrmly attached to the anterior wall of the inferior vena cava, without the possibility of twisting (Fig. 1b). This is an important additional advantage of this technique. The ﬁxation of the liver graft by suturing the round ligament to the recipient abdominal wall optimized graft orientation within the hepatic fossa and additionally prevented its eventual rotation to the right side. The elimination of HVOO was also reported by Heﬀron et al., in a series of 241 consecutive pediatric patients who received 271 hepatic grafts (15). However, 57.6% (156 patients) received whole-sized grafts, 33.2% (90 patients) received deceased donors’ segmental liver transplantations and only 9.2% (25 patients) were livingdonor liver transplantations. The authors reported that the technique of utilizing all three hepatic vein oriﬁces on the recipient hepatic vena cava and the donor hepatic vein cut short enables a wide hepatic outﬂow tract unlikely to twist and eliminated early or late complications of the hepatic vein. The current study compared two large series of liver transplanted patients. The signiﬁcant number of patients and the uniformity of the surgical procedures, which were performed by the same senior surgeon who has performed all operations as the beginning of the liver transplant program, indicate that we may not consider the ﬁrst group of patients as a learning curve. In addition, living-donor liver trans266
plantation is a complex procedure; we therefore judged that the 210 patients included in the current study were suﬃcient for our study. The second study group comprised a large number of patients who showed high rates of success and no complications from our newly proposed technique. This technique represents an important technical innovation in pediatric living-donor liver transplantation. References 1.
DE VILLA VH, CHEN CL, CHEN YS, et al. Outﬂow tract reconstruction in living donor liver transplantation. Transplantation 2000: 70: 1604–1608. NAKAMURA T, TANAKA K, KIUCHI T, et al. Anatomical variations and surgical strategies in right lobe living donor liver transplantation: Lessons from 120 cases. Transplantation 2002: 73: 1896–1903. SAKAMOTO S, EGAWA H, KANAZAWA H, et al. Hepatic venous outﬂow obstruction in pediatric living donor liver transplantation using left-sided lobe grafts: Kyoto University experience. Liver Transpl 2010: 16: 1207–1214. KRISHNA KUMAR G, SHARIF K, MAYER D, et al. Hepatic venous outﬂow obstruction in paediatric liver transplantation. Pediatr Surg Int 2010: 26: 423–425. TANNURI U, MELLO ES, CARNEVALE FC, et al. Hepatic venous reconstruction in pediatric living-related donor liver transplantation - experience of a single center. Pediatr Transplant 2005: 9: 293–298. SAKAMOTO S, NAKAZAWA A, SHIGETA T, et al. Devastating outﬂow obstruction after pediatric split liver transplantation. Pediatr Transplant 2013: 17: E25–E28. BROELSCH CE, LLOYD DM. Living related donors for liver transplantation. Adv Surg 1993: 26: 209–231. HWANG S, LEE SG, LEE YJ, et al. Lessons learned from 1,000 living donor liver transplantations in a single center: How to make living donations safe. Liver Transpl 2006: 12: 920–927. ZHONG J, LEI J, WANG W, YAN L. Systematic review of the safety of living liver donors. Hepatogastroenterology 2013: 60: 252–257. ENGELMANN G, SCHMIDT J, WEITZ J, et al. A new pediatric liver transplantation program in Southern Germany. The Heidelberg experience. Pediatr Transplant 2010: 14: 12–18. KANMAZ T, YANKOL Y, MECIT N, DURMAZ O, ACARLI K, KALAYOGLU M. Pediatric liver transplant: A single-center study of 100 consecutive patients. Exp Clin Transplant 2014: 12: 41–45. GIBELLI NE, TANNURI AC, ANDRADE WC, RICARDI LR, TANNURI U. Centrilobular necrosis as a manifestation of venous outﬂow obstruction in pediatric malnourished liver transplant recipients–case reports. Pediatr Transplant 2012: 16: E383– E387. SOMMOVILLA J, DOYLE MM, VACHHARAJANI N, et al. Hepatic venous outﬂow obstruction in pediatric liver transplantation: Technical considerations in prevention, diagnosis, and management. Pediatr Transplant 2014: 18: 497–502. MAZARIEGOS GV, GARRIDO V, JASKOWSKI-PHILLIPS S, TOWBIN R, PIGULA F, REYES J. Management of hepatic venous obstruction after split-liver transplantation. Pediatr Transplant 2000: 4: 322–327. HEFFRON TG, PILLEN T, SMALLWOOD G, et al. Incidence, impact, and treatment of portal and hepatic venous complications following pediatric liver transplantation: A single-center 12 year experience. Pediatr Transplant 2010: 14: 722–729.
Copyright of Pediatric Transplantation is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.